Neutrophilic Abscesses Research Articles

The efficacy of intensive granulocyte and monocyte adsorption apheresis in a patient with Crohn's disease complicated by extensive subcutaneous aseptic neutrophilic abscesses

Background and aimsSubcutaneous aseptic abscess is one phenotype of neutrophilic dermatitis. We were interested to see if a case of steroid refractory Crohn's disease (CD) complicated by subcutaneous aseptic neutrophilic abscesses responds to intensive granulocyte/monocyte adsorptive apheresis (GMA). MethodsThe patient was a 21-year-old male with worsening severe CD while on oral prednisolone (30mg/day). His symptoms included fever, bloody diarrhoea and multiple painful subcutaneous nodules throughout his body. Skin biopsy showed chronic panniculitis with neutrophilic infiltrates. Further, colonoscopy showed oedematous sigmoid colon, while colonic biopsy showed non-caseous granuloma. Because biologics were feared to increase the risk of bacteraemia as the result of germ culture on his pus was not known at the time, we decided to treat this case with GMA. Five GMA sessions with the Adacolumn over 5 consecutive days (daily GMA) were initiated. ResultsOn admission, his CD activity index (CDAI) was 355, C-reactive protein (CRP) 11.2mg/dL. After 5 GMA sessions, CDAI decreased to 170, and CRP fell to 5.0mg/dL, with no fever. GMA was restarted at 2 sessions/week (total 10 sessions). The patient's CDAI fell to <150, and the skin lesions re-epithelialized. ConclusionsIn this CD case complicated by subcutaneous aseptic neutrophilic abscesses, GMA appeared to be effective. Our impression is that when biopsy reveals neutrophil infiltrate is a major feature of the lesions, GMA should be considered. As GMA appears to have no safety concerns, a frequent GMA protocol, like daily followed by 2 to 3 times/week should be preferred over the routine weekly GMA.

Management of Recalcitrant Hidradenitis Suppurativa with Ustekinumab

Hidradenitis suppurativa (HS) is a chronic inflammatory disease resulting from occlusion of the pilosebaceous units within the intertriginous regions of the body. It is characterized by very tender papules, nodules, and neutrophilic abscesses. Sinus tracts with malodorous drainage and scarring can develop. Long-term complications include lymphoedema and fistulae formation. We present here a difficult case of HS that responded well to ustekinumab.

Alterations in leucocyte subsets and histomorphology in normal-appearing perilesional skin and early and chronic hidradenitis suppurativa lesions

Current insight into the histopathological course of events during disease progression in hidradenitis suppurativa (HS) is fragmentary. To identify histological alterations and leucocyte subsets in normal-appearing perilesional skin, and early and chronic HS lesions. In this observational study we examined eight perilesional skin samples, and six early and 10 chronic prototypic HS lesions, as well as skin samples from four healthy donors using in situ immunostaining. Perilesional skin showed mild psoriasiform hyperplasia and follicular plugging as well as a low-grade influx of tryptase-positive mast cells, CD3+ T cells, CD138+ plasma cells and factor XIIIa+ dendritic cells. In early HS lesions, neutrophilic abscess formation and influx of mainly macrophages, monocytes and dendritic cells predominated. In chronic disease, the infiltrate expanded with markedly increased frequencies of CD20+ and CD79a+ B cells and CD138+ plasma cells. As in early lesions, free keratin fibres were detected in the dermis and within giant cells. Single detached keratinocytes and strands of follicular epithelium were observed in the dermis, the latter frequently expressing Ki67, indicative of active proliferation. Psoriasiform hyperplasia, follicular plugging and low-grade leucocytic infiltration are already present in normal-appearing perilesional skin. Keratin fibres in the dermis are associated with clinical disease. Early lesions are characterized by neutrophilic abscess formation and influx of mainly histiocytes, and chronic lesions mainly by expansion of B cells and plasma cells in 'pseudo' follicles. Proliferating strands of follicular epithelium may initiate fistula formation. Mast cells are increased in all stages of HS including perilesional skin.

Innate and adaptive immune responses against Staphylococcus aureus skin infections

Staphylococcus aureus is an important human pathogen that is responsible for the vast majority of bacterial skin and soft tissue infections in humans. S. aureus can also become more invasive and cause life-threatening infections such as bacteremia, pneumonia, abscesses of various organs, meningitis, osteomyelitis, endocarditis, and sepsis. These infections represent a major public health threat due to the enormous numbers of these infections and the widespread emergence of methicillin-resistant S. aureus (MRSA) strains. MSRA is endemic in hospitals worldwide and is rapidly spreading throughout the normal human population in the community. The increasing frequency of MRSA infections has complicated treatment as these strains are more virulent and are increasingly becoming resistant to multiple different classes of antibiotics. The important role of the immune response against S. aureus infections cannot be overemphasized as humans with certain genetic and acquired immunodeficiency disorders are at an increased risk for infection. Understanding the cutaneous immune responses against S. aureus is essential as most of these infections occur or originate from a site of infection or colonization of the skin and mucosa. This review will summarize the innate immune responses against S. aureus skin infections, including antimicrobial peptides that have direct antimicrobial activity against S. aureus as well as pattern recognition receptors and proinflammatory cytokines that promote neutrophil abscess formation in the skin, which is required for bacterial clearance. Finally, we will discuss the recent discoveries involving IL-17-mediated responses, which provide a key link between cutaneous innate and adaptive immune responses against S. aureus skin infections.

Verrucous carcinoma of the skin: a report on 5 Japanese cases

Verrucous carcinoma (VC) of the skin is relatively rare. The author reports 5 Japanese cases of VC of the skin. The age ranged from 63 to 91 years with a median of 70 years. The locations were hand in 1 case, lip in 1, face in 1, and foot sole in 2. The size ranged from 0.8 cm to 30 mm with a median of 1.5 cm. Grossly, all the cases showed elevated verrucous tumors. Histologically, the tumors were composed of squamous epithelial cells with minimal cellular atypia arranged in a verrucous pattern. One case showed koilocytosis. Neutrophilic abscesses were seen in 3 cases. Microinvasion was recognized in 2 cases. Focus of less differentiated squamous cell carcinoma was seen in the VC in 1 case. Actinic karatosis or squamous cell carcinoma in situ contiguous to VC was seen in 1 case. Definite precedent lesions were not recognized in any of the cases. Immunohistochemically, VCs of the skin were negative for human papilloma virus antigens in the 2 cases examined. p53 protein was expressed in all the VCs and accentuated in the basal and microinvasive parts. The Ki-67 antigen was also expressed in all the VCs, and it was mainly observed in the basal and microinvasive areas. These findings suggest that (1) VC of the skin can occur in any skin sites, (2) VC of the skin can transform into less differentiated squamous cell carcinoma, and (3) VC of the skin may be associated with squamous cell carcinoma in situ.

Subclassification of Autoimmune Pancreatitis

Autoimmune pancreatitis (AIP) is a chronic inflammatory disease of the pancreas. Examination of pancreatic resection specimens from patients with AIP has shown that there are 2 subclasses of this disease. However, there is no widely accepted pathologic classification scheme and the clinical significance of such a classification remains to be established. In this study, we revisited the subclassification of AIP and examine whether this provides clinically and prognostically meaningful information. We evaluated 29 pancreatic resection specimens from patients with AIP. Demographic, clinical, and imaging data were recorded, as was evidence of extrapancreatic manifestations. In addition to a detailed and semiquantitative histologic evaluation, immunohistochemistry for IgG4 was performed on pancreatic and extrapancreatic tissues. We also evaluated 48 consecutive cases of chronic pancreatitis, not otherwise specified. The resected specimens could readily be subclassified into 2 subtypes: type 1 (n=11) and type 2 (n=18). In comparison with patients with type 2 disease, patients with type 1 disease were significantly more likely to be males (P=0.09), older (P=0.02), and present with jaundice (P=0.01), and less likely to be associated with abdominal pain (P=0.04). On imaging, the pancreatic tail cut-off sign was exclusively seen in patients with type 2 disease (4 of 10 cases). Hypercellular inflamed interlobular stroma was unique to type 1 pattern (91%), whereas significant ductal injury in the form of microabscesses and ductal ulceration was almost exclusively seen in type 2 pattern (78%). Eight of 10 patients with a type 1 pattern had evidence of a systemic disease. Three patients with type 2 disease had recurrent episodes of pancreatitis after their pancreatic resection. In comparison with the cohort of chronic pancreatitis, not otherwise specified, type 2 AIP cases were less likely to be associated with a history of alcohol abuse, and showed significantly more foci of periductal inflammation and neutrophilic microabscesses. Our review of pancreatic resection specimens shows 2 histologically distinct forms of AIP. Our data support the concept that type 1 AIP is a systemic disease and is the pancreatic manifestation of IgG4-related systemic disease. Type 2 disease is confined to the pancreas. The intensity of the periductal inflammatory infiltrate and the presence of ductal neutrophilic abscesses are features that assist in distinguishing type 2 AIP from chronic pancreatitis, not otherwise specified. Although imperfect, clinical and imaging features may help distinguish the 2 subtypes of AIP. On the basis of these significant differences between the 2 types of AIP, we advocate the position that all subsequent studies attempt to substratify their patients into these 2 groups.

Primary localized cutaneous amyloidosis intermingled with papulopustular lesions in a patient with Behçet’s disease

Primary localized cutaneous amyloidosis (PLCA) sometimes shows overlapping with collagen vascular diseases; however, association with Behçet's disease (BD) is rare. We herein report a case of PLCA developing intermingled with papulopustular lesions associated with BD. A 57-year-old woman visited our hospital, complaining of recalcitrant multiple oral aphthae. Further detailed physical examination revealed folliculitis-like small pustules with surrounding erythema on the upper back. Also, she stated past histories of genital ulcers 10 years ago and erythema nodosum on the lower legs 4 years ago. A biopsy specimen from the pustular lesion on the back showed neutrophilic abscess in the epidermis with a number of perivascular inflammatory cells in the upper dermis. Congo-red and Dylon stain revealed amyloid deposition in the papillary dermis. Although association of systemic amyloidosis with BD is occasionally found in the literature, co-occurrence of cutaneous amyloidosis and papulopustular lesions of BD is extremely rare.

3 Cases of Dissecting Cellulitis of the Scalp Treated With Adalimumab

Dissecting cellulitis of the scalp (DCS) is a chronic inflammatory disease of scalp hair follicles manifesting as multiple painful nodules and abscesses that interconnect via sinus tracts. The disease tends to run a progressive course that eventually results in scarring alopecia. The condition is thought to represent a follicular occlusion disorder. Sebaceous and keratinous material within dilated pilosebaceous units accumulates until follicles burst, with subsequent neutrophilic inflammatory reaction and abscess formation. Treatment remains unsatisfactory. While oral antibiotics, intralesional corticosteroids, isotretinoin, or dapsone are insufficient, in this case series the inflammation responsible for scarifying tissue destruction was directly targeted by means of the tumor necrosis factor antagonist adalimumab. Observation Clinical signs of inflammation as well as burden of disease measured by a score of 0 to 10 (P < .04) was reduced rapidly by adalimumab. Histopathologic characteristics demonstrated marked improvement of inflammation, despite persistence of underlying structural disease. Relapse was observed following discontinuation of adalimumab. Adalimumab is effective for treatment of DCS. Relapse on discontinuation of therapy can be expected depending on persisting structural disease. Continuous treatment or combined surgical resection of involved areas could be necessary for definitive resolution of disease.

A rare case of septicemia due to Bacteroides melaninogenicus in a Holstein cow

A 6-year-old Holstein cow was referred for necropsy due to sudden death. The necropsy indicated hydroperitoneum, hydropericardium, and petechial hemorrhage on serosal surfaces associated with pulmonary edema and multiple abscesses in the liver. Histopathological examination revealed extensive hepatocellular necrosis with neutrophilic infiltrates and abscess formation. Cultures of the liver lesions and blood revealed a Gram-negative anaerobic bacteria confirmed as Bacteroides melaninogenicus.

Bacillus subtilis induces morphological changes in Fonsecaea pedrosoi in vitro resulting in more resistant fungal forms in vivo

Interactions among microorganisms may be the cause of morphological modifications, particularly in fungal cells. The aim of this work was to examine the changes that occur in cells of the fungus Fonsecaea pedrosoi after in vitro co-culturing with Bacillus subtilis and to explore the results of this interaction in vivo in an experimental murine infection. B. subtilis strain was inoculated into a 15-day pure culture of F. pedrosoi. In vitro, after 48 hours of co-culturing, the fungal cells were roundish. The secretion of fungal dark pigments and production of terminal chlamydoconidia were observed in hyphae after one week. In the in vivo study, two animal groups of 30 BALB/c mice each were employed. One group was inoculated intraperitoneally with hyphal fragments from the co-culture of bacteria and fungi; the other group was infected only with F. pedrosoi hyphae. After seven days of infection, both animal groups developed neutrophilic abscesses. Phagocytosis of bacilli by macrophages occurred at three days. At later periods, generally after 25 days, only roundish cells similar to sclerotic bodies remained in the tissues while hyphae were eliminated by 15 to 20 days. These fungal forms originated mainly from terminal chlamydoconidia. The co-culturing between bacteria and fungi may constitute a mechanism to rapidly obtain resistant fungal forms for host defenses, especially for chromoblastomycosis (CBM) experimental infections.

Acute cellular rejection and its sequelae developing in a 42‐year‐old man after liver transplantation†

A 42-year-old man with alcoholic liver disease underwent successful liver transplantation (LT) using a deceased donor. Both patient and donor were negative for antibody to cytomegalovirus (CMV), and the initial post-LT course was uneventful. Immunosuppression consisted of interleukin-2 antagonist induction as well as tacrolimus, mycophenolate mofetil, and corticosteroids. Corticosteroids were discontinued by month 3 and tacrolimus levels were maintained between 10-15 ng/mL, with infection prophylaxis discontinued 3 months after LT. Following an episode of viral gastroenteritis, the patient became jaundiced with the following laboratory values: alanine aminotransferase 980 U/L, aspartate aminotransferase 810 U/L, alkaline phosphatase 390 U/L, and total bilirubin 15.8 mg/dL. Viral serologies were negative. Abdominal imaging showed no biliary or vascular abnormalities and a liver biopsy was performed that demonstrated severe acute cellular rejection. CMV, cytomegalovirus; LT, liver transplantation. Figure 1 is a representative portal area from the biopsy showing severe inflammation consisting of a mixed infiltrate including eosinophils, plasma cells and lymphocytes, as well as endotheliitis (arrowheads) and bile duct damage (arrow). The patient received pulse corticosteroids as well as thymoglobulin with gradual improvement in the liver chemistry tests over a 3-week period. The tacrolimus dose was optimized and infection prophylaxis was resumed. However, shortly thereafter, the patient was hospitalized with worsening liver chemistry tests and decreasing hematologic indices. CMV as analyzed by polymerase chain reaction was found in high titer, and liver biopsy confirmed the presence of CMV hepatitis. Figure 2 is a representative field from the biopsy demonstrating a cell with the pathognomonic owl-eye nuclear inclusion body (arrow) and intracytoplasmic inclusions that are denoted by arrowheads. Antiviral treatment was initiated and the liver and hematologic abnormalities improved. Within 3 months, however, despite continuing immunosuppression with tacrolimus, mycophenolate and corticosteroids, the liver chemistry tests again worsened: alanine aminotransferase 125 U/L, aspartate aminotransferase 111 U/L, alkaline phosphatase 750 U/L, and total bilirubin 12.9 mg/dL. Another liver biopsy was performed which showed the loss of bile ducts in the majority of portal tracts. Figure 3 is a representative area showing lobular cholestasis and feathery degeneration (arrowhead) as well as a portal tract with an arteriole but without an accompanying bile duct (arrow). This is consistent with bile duct loss and indicative of chronic ductopenic rejection. Cytokeratin 7 immunostaining confirmed greater than 50% bile duct loss. Unfortunately, the patient eventually developed fungemia and expired. A postmortem examination was performed. Figure 4 is a section taken from the liver hilum showing almost total obliteration of the lumen of a hepatic artery by foamy macrophages (arrows) indicative of foam cell arteriopathy. Acute cellular rejection is diagnosed based on the degree of portal inflammation, bile duct damage, and venous endotheliitis.1 Post-LT CMV infection occurs more frequently in patients who have no previous exposure to CMV, especially in the setting of increased immunosuppression.2 Microabscesses are often seen along with the pathognomonic CMV inclusion bodies. These parenchymal neutrophilic abscesses were once thought to be specific for CMV hepatitis but are now known to also occur in the setting of other infections, graft ischemia, and biliary obstruction.3 Both severe acute cellular rejection and CMV infection may predispose to the development of chronic ductopenic rejection.4 Chronic rejection may lead to graft loss with patients most commonly dying from infection. It is characterized by progressive jaundice and obliterative arteriopathy. Cytokeratin staining can give a more accurate count of the degree of bile duct loss; greater than 50% loss is defined as ductopenia. Foam cell arteriopathy often affects larger vessels and is typically not seen on a needle biopsy. Chronic rejection can be classified as either early or late, based on bile duct degenerative changes and loss, hepatic arteriolar loss, and the degree of foam cell arteriopathy in larger arteries.5 Unexplained cholestasis unaccompanied by portal tract changes of biliary obstruction should prompt a careful assessment for subtle bile duct changes suggestive of early chronic rejection.3

Epidermolysis bullosa acquisita: concise review and practical considerations

Introduction Epidermolysis bullosa acquisita (EBA) is a cutaneous subepi-dermal autoimmune blistering disorder (CSEAIBD) that resultsfrom the effects of IgG autoantibodies directed against the145-kDa noncollagenous amino-terminal (NC-1) domain ofcollagen VII, a major component of anchoring fibrils (Fig. 1).

Isolated Renal Nocardiosis in An AIDS Patient: Unusual Presentation with Large Renal Mass

Introduction: Nocardiosis is an acute, subacute or chronic suppurative infection caused by Nocardia. It can be localised or systemic. Localised cutaneous or lymphocutaneous form occurs after an abrasion. Disseminated or systemic infection is seen in immunocompromised individuals. The primary disease occurs in the lung and subsequently haematogenous dissemination may occur to all organs of the body. Case Report: A 55 year old male presented with symptoms of pain in the left loin for 4 years, easy fatiguability since 2 years and fever for 1 year. His pain abdomen was intermittent, crampy and was associated with burning micturition.Two years back the patient was evaluated for extreme fatiguability and was found to be seropositive for HIV and was started on anti-retroviral drugs. His CD4 count was 38 cells/microliter (CD 4% −11.42). CTKUB showed multiple multiple left renal calculi and left ureteric calculi with hydroureter. In view of left non-functioning kiney with stones, nephrectomy was performed. Gross examination of the excised nephro-ureterectomy specimen showed effacement of the entire kidney by tumorous mass with friable necrotic debris along with impacted calculi in the ureter. Microscopic examination showed numerous basophilic filamentous bacterial colonies surrounded by neutrophilic abscesses and dense infiltration by chronic inflammatory cells, which stained positive with acid fast bacilli. Kidney parenchyma showed sclerosed glomeruli, atrophic tubules and dense interstitial inflammatory infiltrate.A diagnosis of Renal nocardiosis was made.A detailed evaluation ruled out pulmonary or systemic involvement. He was started treatment with cotrimoxizole and doxycycline. Discussion: Majority of the cases present as invasive pulmonary infection,disseminated disease or brain abscess. Nocardiosis of kidney is seen in disseminated disease and presents as multiple pyelonephritic microabcesses.Our case had no evidence of pulmonary disease or any other organ involvement. Isolated renal Nocardiosis manifesting as a large tumorous mass is a rare presentation not described in literature to the best of our knowledge.

Sporotrichosis in Uttarakhand (India): a report of nine cases

Sporotrichosis is a chronic granulomatous infection caused by Sporothrichum schenckii. The disease has worldwide distribution. Majority of cases from India are reported from North-eastern states. The demographic, clinico-investigative profile and therapeutic results of nine patients with cutaneous sporotrichosis attending the Dermatology Outdoor Department between January 2005 and June 2006 have been compiled. Out of nine (male-4, female-5) patients, five had lymphocutaneous-type sporotrichosis while four had fixed cutaneous sporotrichosis. The average age of these patients was 40.8 years. The duration of complaints ranged from 1 month to 15 months (average 8.6 months). Two patients were able to recall traumatic injury. Six patients had lesions over lower extremities, two over face and one over upper extremity. Histopathologically, all cases showed granulomatous process with mixed inflammatory infiltrate comprising of lymphocytes, plasma cells, histiocytes and small neutrophil abscesses. Two cases were positive for fungal cells on PAS staining. Fungal culture on skin tissue was positive in all cases. Eight patients were treated with saturated solution of potassium iodide (SSKI) and they responded very well to SSKI in 12-16 weeks. One patient was pregnant and therefore was advised thermotherapy. Sporotrichosis is also present in north-western region of India as it is reported from north-eastern part. This is the first series of cutaneous sporotrichosis being reported from Uttarakhand, a state situated in the north-western region of India.

The cutaneous manifestations of atypical complete DiGeorge syndrome: a histopathologic and immunohistochemical study

DiGeorge syndrome is a congenital anomaly with a constellation of findings that includes thymic hypoplasia. Only a small subset of patients with DiGeorge syndrome has complete athymia, classified as complete DiGeorge anomaly; one third of these patients show an eczematous dermatitis, oligoclonal T-cells and lymphadenopathy, known as atypical complete DiGeorge anomaly. Six biopsies from six patients with the distinctive clinical phenotype of atypical complete DiGeorge anomaly were studied. Every biopsy showed exocytosis (100%), parakeratosis, often confluent and spongiosis (100%). Neutrophilic abscesses (50%), dyskeratosis (67%) and satellite cell necrosis (50%) were seen. Perieccrine and perivascular inflammation were seen in half of the cases. Eosinophils were identified (83%); most commonly in both the epidermis and dermis. All of lymphocytes were CD3 positive. Most (83%) of cases contained T-cell intracellular antigen 1 (TIA-1) positive cells. Special testing of the selected patients using spectratyping identified oligoclonal T-cell populations. The presence of dyskeratotic keratinocytes, satellite cell necrosis and parakeratotic scale with neutrophils characterizes the cutaneous rash seen in this subset of complete DiGeorge syndrome patients. Such skin lesions from patients with DiGeorge anomaly should alert the pathologist to the potential diagnosis of atypical complete DiGeorge anomaly. The pathophysiologic role of the oligoclonal T-cells in this entity requires additional study.

Index of Suspicion

Index of Suspicion

Fatal outcome of pyoderma gangrenosum with multiple organ involvement and partially responding to Infliximab

Abstract Pyoderma gangrenosum is an inflammatory dermatosis of uncertain etiology, often associated with chronic inflammatory bowel or rheumatoid disease. It predominantly affects the skin. A systemic organ involvement caused by aseptic neutrophilic abscesses, however, fundamentally influences the prognosis. A patient with idiopathic pyoderma gangrenosum insufficiently responded to a conventional immune suppressive therapy and the disease proceeded aggressively. During treatment with Infliximab, partial remission was achieved intermediately. However, a recurring endocarditis, led to a lethal outcome of this patient.

NADPH Oxidase Restrains the Matrix Metalloproteinase Activity of Macrophages

Matrix metalloproteinases (MMPs) regulate numerous functions in normal and disease processes; thus, irreversibly blocking their activity is a key step in regulating MMP catalysis. We previously showed in vitro that oxidizing intermediates generated by phagocytes inactivate MMPs by modifying specific amino acids. To assess whether this mechanism operates in vivo, we focused on MMP-12, a macrophage-specific MMP known to mediate emphysema in mouse models. We found that mice lacking gp91(phox), a phagocyte-specific component of the NADPH oxidase, developed extensive, spontaneous emphysematous destruction of their peripheral air spaces, whereas mice deficient in both NADPH oxidase and MMP-12 were protected from spontaneous emphysema. Although gp91(phox)-null and wild-type macrophages produced equivalent levels of MMP-12 protein, the oxidant-deficient cells had greater MMP-12 activity than wild-type macrophages. These findings indicate that reactive intermediates provide a physiological mechanism to protect tissues from excessive macrophage-mediated damage during inflammation.

The first case of cutaneous mucormycosis caused by Rhizopus azygosporus

A rapidly enlarging leg ulcer appeared in a 54-year-old woman with systemic lupus erythematosus receiving aggressive immunosuppressive therapy. Skin biopsy revealed proliferation of hyphae in the midst of a neutrophilic abscess. Culture yielded Rhizopus azygosporus. As no organ involvement was detected by thorough examination, the patient was diagnosed as having primary cutaneous mucormycosis. Although intravenous amphotericin B therapy seemed to be very effective, it had to be discontinued due to nephrotoxicity. She unfortunately died of subsequent disseminated fungal infection and cerebral infarction in which the primary cause could not be determined. Minimum inhibitory concentrations of several antifungal drugs to the isolate were examined and amphotericin B proved to be the only agent that may potentially reach the effective plasma concentration. This is the first case report of cutaneous mucormycosis caused by R. azygosporus.

Fulminant myocarditis demonstrating uncommon morphology?a report of two autopsy cases

Two autopsy cases of fulminant myocarditis demonstrating uncommon morphology were studied. Subjects included two male patients: a 42-year-old (case 1) and a 39-year-old (case 2). Both cases had fever, chest or epigastric pain, electrocardiographic abnormalities, prominent elevation of serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, lactic dehydrogenase and creatine phosphokinase. They were treated with intra-aortic balloon pumping and percutaneous cardiopulmonary support, and they died at 3 days and 4 days after admission (total course of 10 days and 9 days), respectively. Case 1 showed focal necrosis, severe myocardial dystrophic calcification positive for Kossa stain, inflammatory edema, lymphocyte and macrophage infiltration and extravasation of erythrocytes. Case 2 showed acute inflammation and severe myocardial necrosis with neutrophilic abscess, lymphocyte and macrophage infiltration, cell debris and purulent exudate. Calcified, degenerative and necrotic cardiac myocytes and macrophages were reacted with anti-Enterovirus antibody (clone 5-D8/1), which recognizes an epitope on the VP1 peptide of most Coxsackievirus, echovirus, poliovirus and enterovirus strains. Therefore, the present two cases may be compatible with fulminant enterovirus-associated myocarditis. Using reverse transcriptase-semi-nested polymerase chain reaction, picornaviral RNA was detected in the amplified products extracted from the paraffin-embedded myocardial sample of case 1 but not in case 2.